Arrhythmogenic cardiomyopathy (ACM), also known as arrhythmogenic right ventricular cardiomyopathy in particular (ARVC), is associated with a high frequency of arrhythmias and sudden cardiac death (Marcus et al., Circulation 1982; 65:384-98; Thiene et al., N Engl J Med 1988; 318:129-33; Dalal et al., Circulation 2005; 112:3823-32). Mutations in genes encoding desmosomal proteins (including desmoplakin, plakoglobin, plakophilin 2, desmocollin 2, and desmoglein 2) have been identified in approximately 60% of patients with ARVC (te Riele et al., J Cardiovasc Magn Reson. 2014; 16:50). However, genetic analysis remains mainly a research tool, and in everyday practice the diagnosis of ACM can be challenging. The clinical presentation may be highly variable, and the genetic penetrance is often low. This is especially true in family members of an index patient in whom establishing a diagnosis of ACM or ARVC requires extensive clinical workup, often leading to equivocal results. Endomyocardial biopsy has not been consistently useful because the structural changes in ARVC tend to spare the subendocardium and do not typically involve the interventricular septum (Thiene et al., 1988, supra) which are the locations in the heart that are typically sampled during conventional endomyocardial biopsy. Thus, the pathological features of ACM/ARVC are often not seen in conventional endomyocardial-biopsy specimens. Moreover, these pathological features tend to be most conspicuous in patients with severe disease and are not well developed in patients with early disease. In the end, the diagnosis usually rests on fulfilling a set of clinical criteria; see, e.g., Marcus et al., Circulation, 2010; 121:1533-1541. Although these criteria are relatively specific, they are not highly sensitive.